Chronic thromboembolism phenotypes after acute pulmonary embolism: identification with the SEARCH algorithm.

Post‐traumatic stress disorder (PTSD) is a long‐term neuropsychiatric disorder characterized by maladaptive fear processing and affective and cognitive impairment that results after exposure to trauma. Though historically viewed as a purely psychological disorder, there is a growing representative clinical and preclinical body of evidence indicating that PTSD is a disease with an underlying neurobiological pathology of persistent neurobiological dysregulation., Such changes encompass sustained oxidative disequilibrium, continuous neuroinflammatory response, and poor neuroplasticity in the stress‐sensitive brain pathways of the hippocampus, amygdala, and prefrontal cortex., Among the available experimental paradigms, the single prolonged stress (SPS) model is one of the most extensively validated rodent models of post‐traumatic stress disorder (PTSD)., SPS is a reliable model for reproducing key neuroendocrine features of the disorder, such as hypothalamic–pituitary–adrenal (HPA) axis dysregulation, fear extinction impairment, increased anxiety‐like behavior and long‐lasting molecular and structural brain changes., Notably, SPS provokes chronic oxidative stress and neuroinflammatory events in corticolimbic areas, which offer a solid platform to challenge experimental treatments that act on convergent pathological pathways rather than single neurotransmitter systems., , The growing body of evidence suggests that neuroinflammation and oxidative stress can be the primary mechanisms of PTSD chronicity rather than an epiphenomenal consequence., Sustained elevations of pro‐inflammatory cytokines, such as interleukin 1β (IL‐1β), IL‐6, and tumor necrosis factor α (TNF‐α), increased lipid peroxidation products, and decreased antioxidant enzyme activity have consistently been observed in PTSD patients and rodents exposed to SPS., Those molecular disruptions are intertwined with astrocytic reactivity, neuronal susceptibility, and lowering of brain‐derived neurotrophic factor (BDNF) that are all related to impeded synaptic plasticity, structural fragility, and behavioral rigidity., , ,